|Lei, Xin Gen|
Submitted to: Journal of Nutrition
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/5/2007
Publication Date: 10/20/2007
Citation: Yasuda, K., Maiorano, R., Welch, R.M., Miller, D., Lei, X. 2007. Cecum is the major degradation stie of ingested inulin. Journal of Nutrition. 137:399-2404. Interpretive Summary: Certain non-digestible carbohydrates, such as inulin, are known to be prebiotics that stimulate the growth of beneficial microorganisms in the hind gut of monogastric animals including humans. Pig models have been used to study the effects of prebiotics on gut health but have been criticize because they may digest prebiotics in the small intestine thus differing from humans who digest prebiotics primarily in the large intestine. We determined where the prebiotic, inulin, is digested in the pig gut. We report that, as in humans, pigs digest inulin primarily in the large intestine and not in the small intestine showing that the pig model is a good model for studying the effects of prebiotics on gut health in humans.
Technical Abstract: Abstract Two groups have reported > 90% of pre-caecal digestibility of inulin in pigs, and argued against pigs as a proper animal model for humans in this regard. Two experiments were conducted with weanling pigs to characterize the complete hydrolysis profile of inulin in various segments of the entire GI tract. In Exp. 1, 12 pigs (7.7 +/- 0.2 kg of body weight) were fed the low-iron (54 mg/kg) BD or BD + 4% inulin (Synergy 1, Orafti, Tienen, Belgium) for 6 wk. All pigs were killed at the end of the trial to collect digesta samples from stomach, upper and lower jejunum, cecum, and proximal, mid, and distal colon. Inulin was detected only in digesta from the first three segments (0.4 to 5.5%, dry basis), but not from the large intestine of pigs fed inulin. Fructose concentrations in digesta from stomach and jejunum were greater (P < 0.05) in pigs fed inulin than those fed BD. To further determine if and how inulin was degraded mainly in ileum or cecum, we conducted Exp. 2 with 12 pigs (11.2 ' 1.1 kg of body weight) for 8 wk as did in Exp.1. except that ileum instead of upper jejunum digesta samples were collected. Likewise, inulin was detected only in digesta from stomach, jejunum, and ileum of pigs fed inulin. Although the activity of inulin degrading enzymes was detectable in digesta from ileum, cecum, and proximal colon of both groups, the highest activity (P < 0.05) was found in the cecum digesta of pigs fed inulin. Only digesta from cecum and colon, but not from ileum, was able to degrade added inulin in in vitro incubations. In conclusion, supplemental dietary inulin in pigs was degraded mainly in cecum. Similar to humans, pigs had very limited hydrolysis of ingested inulin in the upper GI tracts from stomach to ileum.